The morphologic features and physiologic mechanisms which are responsible for the recovery process following acute renal injury will be studied. The models to be used will include acute renal failure induced by dichromate administration or by bilateral renal artery occlusion, and the acute renal injury following acute unilateral or bilateral ureteral obstruction. It is proposed to determine the glomerular filtration dynamics and vascular resistance profile of the renal cortex during recovery in order to elucidate the role of these factors in the glomerular-tubular imbalance with results in the diuresis of recovery. Further, it is proposed to evaluate the role of hemodynamic factors, including vasoconstriction, possibly induced by the renin-angiotensin system, or vasodilation mediated by prostaglandins in the pathogenesis of this state. The mechanism of action of magnesium chloride-ATP on the recovery process will also be studied in an attempt to assess the mechanism of action of this complex in accelerating the recovery from acute ischemic renal injury.